Compared with HD BCP-ALL, ETV6::RUNX1+ BCP-ALL harbored on average 3 times more SVs (mainly focal deletions) that might be associated with hyperactive RAG1/2 mediated recombination, which has been described as an oncogenic process in this specific subgroup.38 By contrast, there are limited analyses of aberrant RAG activity in HD BCP-ALL, and mechanisms of secondary SVs need to be further investigated. The gene discussed is RAG1; the disease is acute lymphoblastic leukemia.